Biology:mir-181 microRNA precursor

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mir-181 microRNA precursor
RF00076.jpg
Predicted secondary structure and sequence conservation of mir-181
Identifiers
SymbolmiR-181
RfamRF00076
miRBaseMI0000269
miRBase familyMIPF0000007
Other data
RNA typeGene; miRNA
Domain(s)Eukaryota
GO0035195 0035068
SO0001244
PDB structuresPDBe

In molecular biology miR-181 microRNA precursor is a small non-coding RNA molecule. MicroRNAs (miRNAs) are transcribed as ~70 nucleotide precursors and subsequently processed by the RNase-III type enzyme Dicer to give a ~22 nucleotide mature product. In this case the mature sequence comes from the 5' arm of the precursor. They target and modulate protein expression by inhibiting translation and / or inducing degradation of target messenger RNAs. This new class of genes has recently been shown to play a central role in malignant transformation. miRNA are downregulated in many tumors and thus appear to function as tumor suppressor genes.[1] The mature products miR-181a, miR-181b, miR-181c or miR-181d are thought to have regulatory roles at posttranscriptional level, through complementarity to target mRNAs.[2] miR-181 has been predicted or experimentally confirmed in a wide number of vertebrate species such as rat, zebrafish, and pufferfish (see below) (MIPF0000007).

Expression

It has been shown that miR-181 is preferentially expressed in the B-lymphoid cells of mouse bone marrow,[3] but also in the retina and brain.[4] In humans, this microRNA is involved in the mechanisms of immunity, and in many different cancers (see below) it was found to be expressed at a particularly low level.[5]

Genome location

Human
miR-181a1 and miR-181b1 are clustered together and located on the chromosome 1 (37.p5), miR-181a2 and miR-181b2 are clustered together and located on the chromosome 9 (37.p5).[6][7][8] miR-181c and miR-181d are clustered together and located on the chromosome 19 (37.p5).[2][9][10]

Organisms

miR-181 family are present in vertebrates and nematodes[citation needed] (this list is not exhaustive):


  • lizard (Anolis carolinensis),[11]
  • cow (Bos taurus),[12][13]
  • common carp (Cyprinus carpio),[14]
  • dog (Canis familiaris),[15]
  • Chinese hamster (Cricetulus griseus),[16]
  • zebrafish (Danio rerio),[2]
  • horse (Equus caballus),[17]
  • the pufferfish (Fugu rubripes),
  • chicken (Gallus gallus),[18][19]
  • gorilla (Gorilla gorilla),[20]
  • woolly monkey (Lagothrix lagotricha),[20]
  • short-tailed opossum (Monodelphis domestica),[21]
  • rhesus macaque (Macaca mulatta),[20]
  • mouse (Mus musculus),[22]
  • pig-tailed macaque (Macaca nemestrina),[20]
  • platypus (Ornithorhynchus anatinus),[23]
  • medaka (Oryzias latipes),[24]
  • sea lamprey (Petromyzon marinus),[25]
  • bonobo (Pan paniscus),[20]
  • orangutan (Pongo pygmaeus),[20]
  • chimpanzee (Pan troglodytes),[20]
  • rat (Rattus norvegicus),[26]
  • tasmanian devil (Sarcophilus harrisii),[27]
  • wild boar (Sus scrofa),[20]
  • white-lipped tamarin (Saguinus labiatus),[28]
  • zebra finch (Taeniopygia guttata),[29]
  • tetraodon (Tetraodon nigroviridis),
  • western clawed frog (Xenopus tropicalis),[30]
  • human (Homo sapiens).[2]


miR-181

Chronic lymphocytic leukemia

miR-181 may have a regulatory role with tumor suppressors genes of the human chromosome 1.[5] It has been shown that the Tcl1 oncogene is a target of miR-181a in an inhibition relation (downregulated) that would result in an action on the tumor cell growth process. miR-181 expression has a reverse correlation with Tcl1 protein expression.[31]

Neuroblastoma

mir-181 a and b are over-expressed and act as bad prognosis maker of aggressive neuroblastoma (Stage 4) as compare to low grade stage (Stage 1;2;3 and 4S) whereas mir-181 c and d isoforms are not. In these conditions, they regulate the tumor suppressor gene CDON.[32]

Myoblast differentiation

It has been shown that miR-181 targets the homeobox protein Hox-A11 and participates in establishing muscle tissue downregulating it (a repressor of the differentiation process in mammalians and lower organisms).[33]

Breast cancer

miR-181a, miR-181b, miR-181c and miR-181d are activated by the human gene ERBB2, located on the chromosome 17. The expression of miR-181c is relevant to characterize a Breast cancer form, the HER2/neu.[34]
miR-181 is also activated by the small molecule tamoxifen.[35] One selective modulators of estrogen receptor having specific activities of tissue. Tamoxifen acts as an anti-estrogen (inhibitor) in breast tissue, but as an estrogen (stimulating agent) in cholesterol metabolism, bone density, and the proliferation of endometrial cells. miR-181 could acquire a resistance to tamoxifen, the drug is successfully used to treat women with estrogen receptor-positive breast cancer.[35]

Acute myeloid leukemia

Downregulation of miR-181 family contributes to aggressive leukemia phenotype through mechanisms related to the activation pathways of innate immunity mediated by toll-like receptors TLR2, TLR4, TLR7 and TLR8 and interleukin-1β IL1B (humans on chromose 2).[1]

Glioblastoma

miR-181a, miR-181b, and miR-181c, which are down-regulated in glioblastoma.[36] miR-181b is downregulated in glioma samples compared with the normal brain tissue. It is suggested that the downregulation of miR-181 may play a role in the development of cancer. It is shown that transfection of miR-181a and miR-181b triggers growth inhibition, apoptosis and inhibits invasion. In addition, the expression of miR-181a was found to be inversely correlated with tumor grading while miR-181b was uniformly downregulated in gliomas with different grades of malignancy.[37]

Glioma

It has been shown that downregulated miR-181a and miR-181b were also involved in the oncogenesis of gliomas. miR-181a and miR-181b function as tumor suppressors that cause inhibition of growth, induce apoptosis and inhibit invasion of glioma cells. In addition, the tumor suppressive effect of miR-181b in glioma cells was apparent that the effect of miR-181a. These aberrant results suggest that downregulated miR-181a and miR-181b may be key factors that contribute to the occurrence in malignant human gliomas.[38]

Multiple myeloma

MiRNA signature for multiple myeloma (MM) has been described, including miR-181a and miR-181b, which modulate the expression of proteins essential for the pathogenesis of myeloma. Xenograft studies using human MM cell lines treated with miR-181a and miR-181b antagonists resulted in significant suppression of tumor growth in nude mice.[39]

Papillary thyroid carcinoma

It was found that miR-181a and miR-181c are overexpressed in Papillary Thyroid Carcinoma tumors, sufficiently to successfully predict cancer status.[40]

Hepatocellular carcinoma

It has been shown that conserved miR-181 family were upregulated in EpCAM+ AFP+ Hepatocellular carcinoma (HCC) cells and EpCAM+ HCC isolated from AFP+ tumors. In addition, miR-181 family members were highly expressed in the embryonic liver and isolated hepatic stem cells. Especially, inhibition of miR-181 leads to a reduction of the EpCAM+, the amount of HCC cells and initiate tumor capacity, whereas exogenous miR-181 expression in HCC cells resulted in an enrichment of EpCAM+ HCC cells. miR-181 could directly target hepatic transcriptional regulators of differentiation (like homeobox 2 CDX2 and 6 GATA proteins binding GATA6) and an inhibitor of Wnt / beta-catenin. It suggests that miR-181 may eradicate HCC.[41]

miR-181a

T-cell sensitivity

The increased expression of miR-181a in mature T cells increases susceptibility to peptide antigens, while inhibiting the expression of miR-181a in immature T cells reduces sensitivity and alters the both positive and negative selection. In addition, the quantitative regulation of the sensitivity of T cells by miR-181a allows for mature T cells recognize peptide inhibitor antagonists, like agonists. These effects are achieved in part by downregulation of multiple phosphatases, which leads to high levels of steadystate phosphorylated intermediates and reducing the threshold of T cell receptor signaling. The expression of miR-181a correlates with a greater sensitivity of immature T cells in T cells, suggesting that miR-181a acts as an antigen intrinsic sensitivity "rheostat" during the development of T cells.[42]

Vascular development

It has been shown that miR-181a binds the 3' UTR of Prox1 leading to translation repression and transcript degradation. Prox1 is a homeobox transcription factor involved in development of the lymphatic endothelium.[43]

Cerebellar neurodegeneration

miR-181a has a relatively broad expression pattern and is present in neurons in numerous parts of the mouse brain. miR-181a is essential for the survival of Purkinje cells and its absence leads to a slow degeneration of these cells.[44]

Diabetes mellitus

It has been shown that there are significant correlations between the expression of miR-181a and both adipose tissue morphology and key metabolic parameters, including visceral fat area, HbA1c, fasting plasma glucose, and circulating leptin, adiponectin, interleukin-6. The expression of miR-181a may contribute to intrinsic differences between omental and subcutaneous adipose tissue.[45]

Homozygous sickle cell disease

miR-181a is over-represented in the normal hemoglobin (HbAA) erythrocytes.[46] miR-181a has been shown to play a role in the lineage differentiation in the hematopoietic system.[3]

Breast cancer

miR-181a expression is associated with survival in triple negative breast cancer. Patients with low expression have lower probability of survival over time.[47]

miR-181b

Colorectal cancer

miR-181b was significantly overexpressed in tumors compared to normal colorectal samples, especially high miR-181b expression correlated with poor survival of only black patients with stage III colorectal cancers [48] (Sequencing analysis revealed that miR-181b expression is strongly associated with mutation status of the tumor suppressor gene p53.[49]

Cardiac hypertrophy

miR-181b is downregulated during hypertrophy, it causes a reduction in cardiomyocyte cell size.[50]

Oral carcinoma

miR-181b expression was steadily increased and is associated with increased severity of lesions during the progression of the Oral Carcinoma. Overexpression of miR-181b may play an important role in malignant transformation.[51]

Prostate cancer

miR-181b is downregulated in cancerous cells.[52]

Adrenocortical carcinoma

Mir-210 has been suggested as a useful biomarker to distinguish adrenocortical carcinoma from adrenocortical adenoma.[53]

miR-181c

miR-181d

Duchenne muscular dystrophy

miR-181d is disregulated in Duchenne muscular dystrophy (DMD).[54]

Nemaline myopathy

miR-181d is disregulated in nemaline myopathy (NM).[54]

References

  1. ↑ 1.0 1.1 "Micro-RNAs and copy number changes: new levels of gene regulation in acute myeloid leukemia". Chemico-Biological Interactions 184 (1–2): 21–5. March 2010. doi:10.1016/j.cbi.2009.10.002. PMID 19822134. 
  2. ↑ 2.0 2.1 2.2 2.3 "Vertebrate microRNA genes". Science 299 (5612): 1540. March 2003. doi:10.1126/science.1080372. PMID 12624257. 
  3. ↑ 3.0 3.1 "MicroRNAs modulate hematopoietic lineage differentiation". Science 303 (5654): 83–6. January 2004. doi:10.1126/science.1091903. PMID 14657504. 
  4. ↑ "MicroRNAs of the mammalian eye display distinct and overlapping tissue specificity". Molecular Vision 12: 1175–84. October 2006. PMID 17102797. 
  5. ↑ 5.0 5.1 "Small RNAs analysis in CLL reveals a deregulation of miRNA expression and novel miRNA candidates of putative relevance in CLL pathogenesis". Leukemia 22 (2): 330–8. February 2008. doi:10.1038/sj.leu.2405022. PMID 17989717. 
  6. ↑ "Patterns of known and novel small RNAs in human cervical cancer". Cancer Research 67 (13): 6031–43. July 2007. doi:10.1158/0008-5472.CAN-06-0561. PMID 17616659. 
  7. ↑ "Kaposi's sarcoma-associated herpesvirus expresses an array of viral microRNAs in latently infected cells". Proceedings of the National Academy of Sciences of the United States of America 102 (15): 5570–5. April 2005. doi:10.1073/pnas.0408192102. PMID 15800047. 
  8. ↑ "Numerous microRNPs in neuronal cells containing novel microRNAs". RNA 9 (2): 180–6. February 2003. doi:10.1261/rna.2141503. PMID 12554860. 
  9. ↑ "A mammalian microRNA expression atlas based on small RNA library sequencing". Cell 129 (7): 1401–14. June 2007. doi:10.1016/j.cell.2007.04.040. PMID 17604727. 
  10. ↑ "Identification of hundreds of conserved and nonconserved human microRNAs". Nature Genetics 37 (7): 766–70. July 2005. doi:10.1038/ng1590. PMID 15965474. 
  11. ↑ "MicroRNAs support a turtle + lizard clade". Biology Letters 8 (1): 104–7. February 2012. doi:10.1098/rsbl.2011.0477. PMID 21775315. 
  12. ↑ "Annotation of 390 bovine miRNA genes by sequence similarity with other species". Animal Genetics 40 (1): 125. February 2009. doi:10.1111/j.1365-2052.2008.01780.x. PMID 18945293. 
  13. ↑ "Characterization of bovine miRNAs by sequencing and bioinformatics analysis". BMC Molecular Biology 10: 90. September 2009. doi:10.1186/1471-2199-10-90. PMID 19758457.  open access
  14. ↑ "Identification and profiling of microRNAs from skeletal muscle of the common carp". PLOS ONE 7 (1): e30925. 2012. doi:10.1371/journal.pone.0030925. PMID 22303472.  open access
  15. ↑ "Discovering microRNAs from deep sequencing data using miRDeep". Nature Biotechnology 26 (4): 407–15. April 2008. doi:10.1038/nbt1394. PMID 18392026. 
  16. ↑ "Next-generation sequencing of the Chinese hamster ovary microRNA transcriptome: Identification, annotation and profiling of microRNAs as targets for cellular engineering". Journal of Biotechnology 153 (1–2): 62–75. April 2011. doi:10.1016/j.jbiotec.2011.02.011. PMID 21392545. 
  17. ↑ "In silico detection and characteristics of novel microRNA genes in the Equus caballus genome using an integrated ab initio and comparative genomic approach". Genomics 94 (2): 125–31. August 2009. doi:10.1016/j.ygeno.2009.04.006. PMID 19406225. 
  18. ↑ International Chicken Genome Sequencing Consortium (December 2004). "Sequence and comparative analysis of the chicken genome provide unique perspectives on vertebrate evolution". Nature 432 (7018): 695–716. doi:10.1038/nature03154. PMID 15592404. https://escholarship.org/content/qt44v0c3r5/qt44v0c3r5.pdf?t=or4mqz. 
  19. ↑ "MicroRNA profile of Marek's disease virus-transformed T-cell line MSB-1: predominance of virus-encoded microRNAs". Journal of Virology 82 (8): 4007–15. April 2008. doi:10.1128/JVI.02659-07. PMID 18256158. 
  20. ↑ 20.0 20.1 20.2 20.3 20.4 20.5 20.6 20.7 "Phylogenetic shadowing and computational identification of human microRNA genes". Cell 120 (1): 21–4. January 2005. doi:10.1016/j.cell.2004.12.031. PMID 15652478. 
  21. ↑ "In vitro and in silico annotation of conserved and nonconserved microRNAs in the genome of the marsupial Monodelphis domestica". The Journal of Heredity 99 (1): 66–72. 2008. doi:10.1093/jhered/esm085. PMID 17965199. 
  22. ↑ "New human and mouse microRNA genes found by homology search". The FEBS Journal 272 (1): 59–73. January 2005. doi:10.1111/j.1432-1033.2004.04389.x. PMID 15634332. 
  23. ↑ "Conservation of small RNA pathways in platypus". Genome Research 18 (6): 995–1004. June 2008. doi:10.1101/gr.073056.107. PMID 18463306. 
  24. ↑ "Discovery and characterization of medaka miRNA genes by next generation sequencing platform". BMC Genomics 11 (Suppl 4): S8. December 2010. doi:10.1186/1471-2164-11-S4-S8. PMID 21143817.  open access
  25. ↑ "microRNAs reveal the interrelationships of hagfish, lampreys, and gnathostomes and the nature of the ancestral vertebrate". Proceedings of the National Academy of Sciences of the United States of America 107 (45): 19379–83. November 2010. doi:10.1073/pnas.1010350107. PMID 20959416. 
  26. ↑ "Small RNA expression and strain specificity in the rat". BMC Genomics 11: 249. April 2010. doi:10.1186/1471-2164-11-249. PMID 20403161.  open access
  27. ↑ "The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer". Science 327 (5961): 84–7. January 2010. doi:10.1126/science.1180616. PMID 20044575. 
  28. ↑ "Cloning, characterization and expression analysis of porcine microRNAs". BMC Genomics 10: 65. February 2009. doi:10.1186/1471-2164-10-65. PMID 19196471.  open access
  29. ↑ "The genome of a songbird". Nature 464 (7289): 757–62. April 2010. doi:10.1038/nature08819. PMID 20360741. 
  30. ↑ "Xenopus microRNA genes are predominantly located within introns and are differentially expressed in adult frog tissues via post-transcriptional regulation". Genome Research 18 (1): 104–12. January 2008. doi:10.1101/gr.6539108. PMID 18032731. 
  31. ↑ "Tcl1 expression in chronic lymphocytic leukemia is regulated by miR-29 and miR-181". Cancer Research 66 (24): 11590–3. December 2006. doi:10.1158/0008-5472.CAN-06-3613. PMID 17178851. 
  32. ↑ "Regulation by miR181 family of the dependence receptor CDON tumor suppressive activity in neuroblastoma". Journal of the National Cancer Institute 106 (11): dju318. November 2014. doi:10.1093/jnci/dju318. PMID 25313246. 
  33. ↑ "The microRNA miR-181 targets the homeobox protein Hox-A11 during mammalian myoblast differentiation". Nature Cell Biology 8 (3): 278–84. March 2006. doi:10.1038/ncb1373. PMID 16489342. 
  34. ↑ "MicroRNA signatures predict oestrogen receptor, progesterone receptor and HER2/neu receptor status in breast cancer". Breast Cancer Research 11 (3): R27. 2009. doi:10.1186/bcr2257. PMID 19432961. 
  35. ↑ 35.0 35.1 "MicroRNA-221/222 confers tamoxifen resistance in breast cancer by targeting p27Kip1". The Journal of Biological Chemistry 283 (44): 29897–903. October 2008. doi:10.1074/jbc.M804612200. PMID 18708351. 
  36. ↑ "Extensive modulation of a set of microRNAs in primary glioblastoma". Biochemical and Biophysical Research Communications 334 (4): 1351–8. September 2005. doi:10.1016/j.bbrc.2005.07.030. PMID 16039986. 
  37. ↑ "miR-21 and 221 upregulation and miR-181b downregulation in human grade II-IV astrocytic tumors". Journal of Neuro-Oncology 93 (3): 325–32. July 2009. doi:10.1007/s11060-009-9797-4. PMID 19159078. 
  38. ↑ "hsa-mir-181a and hsa-mir-181b function as tumor suppressors in human glioma cells". Brain Research 1236: 185–93. October 2008. doi:10.1016/j.brainres.2008.07.085. PMID 18710654. 
  39. ↑ "MicroRNAs regulate critical genes associated with multiple myeloma pathogenesis". Proceedings of the National Academy of Sciences of the United States of America 105 (35): 12885–90. September 2008. doi:10.1073/pnas.0806202105. PMID 18728182. 
  40. ↑ "The role of microRNA genes in papillary thyroid carcinoma". Proceedings of the National Academy of Sciences of the United States of America 102 (52): 19075–80. December 2005. doi:10.1073/pnas.0509603102. PMID 16365291. 
  41. ↑ "Identification of microRNA-181 by genome-wide screening as a critical player in EpCAM-positive hepatic cancer stem cells". Hepatology 50 (2): 472–80. August 2009. doi:10.1002/hep.22989. PMID 19585654. 
  42. ↑ "miR-181a is an intrinsic modulator of T cell sensitivity and selection". Cell 129 (1): 147–61. April 2007. doi:10.1016/j.cell.2007.03.008. PMID 17382377. 
  43. ↑ "Prox1 expression is negatively regulated by miR-181 in endothelial cells". Blood 116 (13): 2395–401. September 2010. doi:10.1182/blood-2009-12-256297. PMID 20558617. 
  44. ↑ "Cerebellar neurodegeneration in the absence of microRNAs". The Journal of Experimental Medicine 204 (7): 1553–8. July 2007. doi:10.1084/jem.20070823. PMID 17606634. 
  45. ↑ "MicroRNA expression in human omental and subcutaneous adipose tissue". PLOS ONE 4 (3): e4699. 2009. doi:10.1371/journal.pone.0004699. PMID 19259271.  open access
  46. ↑ "The genomic analysis of erythrocyte microRNA expression in sickle cell diseases". PLOS ONE 3 (6): e2360. June 2008. doi:10.1371/journal.pone.0002360. PMID 18523662.  open access
  47. ↑ "miRpower: a web-tool to validate survival-associated miRNAs utilizing expression data from 2178 breast cancer patients" (in en). Breast Cancer Research and Treatment 160 (3): 439–446. December 2016. doi:10.1007/s10549-016-4013-7. PMID 27744485. 
  48. ↑ "The prognostic value of microRNAs varies with patient race/ethnicity and stage of colorectal cancer". Clinical Cancer Research 19 (14): 3955–65. July 2013. doi:10.1158/1078-0432.CCR-12-3302. PMID 23719259. 
  49. ↑ "Prognostic Values of microRNAs in Colorectal Cancer". Biomarker Insights 2: 113–121. 2006. PMID 18079988. 
  50. ↑ "A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure". Proceedings of the National Academy of Sciences of the United States of America 103 (48): 18255–60. November 2006. doi:10.1073/pnas.0608791103. PMID 17108080. 
  51. ↑ "Identification of a microRNA signature associated with progression of leukoplakia to oral carcinoma". Human Molecular Genetics 18 (24): 4818–29. December 2009. doi:10.1093/hmg/ddp446. PMID 19776030. 
  52. ↑ "Diagnostic and prognostic implications of microRNA profiling in prostate carcinoma". International Journal of Cancer 126 (5): 1166–76. March 2010. doi:10.1002/ijc.24827. PMID 19676045. 
  53. ↑ "Analysis of circulating microRNAs in adrenocortical tumors". Laboratory Investigation; A Journal of Technical Methods and Pathology 94 (3): 331–9. March 2014. doi:10.1038/labinvest.2013.148. PMID 24336071. 
  54. ↑ 54.0 54.1 "Distinctive patterns of microRNA expression in primary muscular disorders". Proceedings of the National Academy of Sciences of the United States of America 104 (43): 17016–21. October 2007. doi:10.1073/pnas.0708115104. PMID 17942673. 

Further reading

External links



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